ミオシンに依存した交差点改造は,平面細胞のインターキャラと軸の延長を制御します
Claire Bertet1, Lawrence Sulak, Thomas Lecuit
1Laboratoire de Génétique et de Physiologie du Développement, Institut de Biologie du Développement de Marseille, CNRS-INSERM-Université de la Méditerranée, Campus de Luminy, case 907, 13288 Marseille cedex 9, France.
Nature
|June 11, 2004
まとめ
細胞のインターカレーションは,細胞の結節を再構成することによって,上皮質の形態変異を駆動する. ミオシンIIの活性性は,このプロセスにとって極めて重要であり,組織発達の一般的なモデルを提供します.
科学分野:
- 発達生物学 発達生物学とは
- 細胞生物学 細胞生物学
- バイオフィジックス 生物物理学
背景:
- 組織の形成 (形質変異) は,細胞分裂,形状,およびインターキャレーションによる隣人変化に依存しています.
- アデレンス・ジャンクションによって維持される上皮質の整合性は,インターキャレーションにユニークな課題をもたらします.
研究 の 目的:
- ポラライズされた上皮質の形態変異を駆動する細胞の秩序あるインターカレーションのメカニズムを解明する.
- ドロソフィラの胚における生殖帯の延長における細胞の結合と力の役割を理解する.
主な方法:
- ドロソフィラ胚の細胞インターキャレーション中のジャンクションリモデリングを調査した.
- 平面交差点の改造における局所力とミオシンIIの役割を分析した.
主要な成果:
- 細胞のインターカレーションは,アデレンス接合の空間的再編成によって進行する.
- 平面交差点の改造は,外部の組織力ではなく,局所的な力によって引き起こされます.
- ミオシンIIは,解体接合点で濃縮され,平面リモデリングとインターキャレーションに不可欠です.
結論:
- ポラライズされた表 epithelial morphogenesisのための新しい細胞メカニズムが提案されています.
- 局所的な力とミオシンII依存の交差点改造 駆動細胞のインターキャレーション.
- このメカニズムは,上皮器官の発達の一般的なモデルを提供します.
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